Basic Informations

C.V

Curriculum Vitae

Master Title

Gross anatomical studies on the liver of the goats?

Master Abstract

The present study was conducted on the livers of 80 adult apparently healthy goat of sexes and different ages as well as 7 adult goats and 3 young goats. The topography of the liver was investigated and revealed that the ligaments were divided into visceral and parietal groups. The former, includes, lesser omentum and hepatorenal ligament, while the parietal group constituting, the right triangular ligament, left triangular ligament, coronary, falciform and round ligaments. The morphological aspect of the liver also was revealed that, there were two surfaces; visceral and parietal and four bourders; right, left, dorsal and ventral. The lobes of the liver in our findings were four main lobes; right, left, quadrate and caudate lobe. The latter was divided into caudate and papillary processes. The portal vein, hepatic veins and bile duct was injected by colored latex, cast material (Epoxy 150) and radio-opaque mass (mercury) to be found that:- 1- The portal vein was divided at Porta hepatis into; R. dexter, R. sinister, R. dorsalis dexter and R. omentalis caudalis. It is also noted that there are no valves in the portal vein or its large branches. 2- The hepatic artery was divided into three main branches at Porta hepatis; R. dexter, R. dorsalis dexter and R. sinister. 3-Two main veins, left and middle in addition to vein of caudate process and right hepatic veins established the venous drainage of the livr. 4- The bile duct was formed by the union of left hepatic duct and a short common trunk formed by right and cystic ducts. The bile duct opened in the duodenal papilla 24-27 cm from the pylorus. The results obtained were discussed with those recorded in the other domestic animals. Nomina anatomica Veterinaria (1994) as well as those given by available literatures adopted the nomenclature used in the current investigation.

PHD Title

Effects of hypothyroidism on programmed cell death in forebrain structures of the rat during development and in the adult?

PHD Abstract

Thyroid hormones (thyroxine, T4 and triiodothyronine, T3) play a pivotal role in differentiation, growth, and metabolism of nearly all tissues. In the brain, they have multiple actions on neurogenesis, neuronal cell migration and differentiation, synaptogenesis and myelination. Hypothyroidism during development results in profound mental retardation, deaf-mutism, and spastic diplegia, known in humans as cretinism. Adult thyroid dysfunction is also associated with both neurological and behavioral abnormalities. Recent studies relate hypothyroidism with programmed cell death (apoptosis) during brain development. This study aimed to evaluate the effect of hypothyroidism on cell survival in developing and adult rat forebrain structures in two experimental models of pharmacologically induced hypothyroidism; one with congenital and the other with acquired hypothyroidism. The selected brain areas for studying hypothyroidism were the striatum and the lateral septum. Congenital hypothyroidism was pharmacologically induced by giving dams methimazole in their drinking water from the 9th gestational day and afterwards until the neonatal rats were sacrificed. Acquired hypothyroidism was pharmacologically induced by 4.5 weeks of treatment with methimazole in their drinking water, from postnatal day 35 until sacrifice. We used the TUNEL method for the in situ labeling of DNA fragmentation in dying cells. In addition, we used immunohistochemistry to detect the expression of the reliable apoptotic marker active caspase-3. Immunohistochemistry for GABA was used to examine the effect of hypothyroidism on the survival and phenotype of striatal neurons. For quantitative analysis, we also used cresyl violet staining (Nissl staining method) to determine the number of “live” cells in the striatum and the lateral septum of hypothyroid and normal animals. The results of the present study showed that, hypothyroidism induces apoptotic cell death in the rat forebrain structures during development and in the adult. The apoptotic cell death is mediated by the activation of active caspase-3. Specifically, congenital hypothyroidism significantly increases the density of apoptotic cells in the developing striatum and lateral septum, compared to normal control animals. Our observations based on morphological criteria suggested that most dying cells were of neuronal origin. Congenital hypothyroidism also affects the number of “live” cells, reducing their normal density after birth in the two brain areas examined. On the contrary, acquired hypothyroidism increases the normal density of “live” cells in the above brain areas. Apoptotic neurons, which were never detected in normal adult animals, are present in almost all forebrain structures of adult hypothyroid animals. Our findings also revealed that the density of GABAergic cells in both groups of hypothyroid animals is significantly reduced (about 13.13%) compared to the density of normal control animals. The size of the striatum in adult animals with congenital hypothyroidism is also significantly reduced, compared to normal control animals. On the contrary, in animals with acquired hypothyroidism the corresponding size of the striatum was not affected. Finally, cell survival is dependent on the onset and duration of hypothyroidism. The results of the present study lead to the following conclusions: 1) congenital hypothyroidism augments apoptotic cell death in the developing striatum and lateral septum; 2) congenital hypothyroidism affects the number of “live” cells, through the reduction of their normal density after birth in thestriatum and the lateral septum; 3) congenital and acquired hypothyroidism induce apoptotic cell death in the adult forebrain, wich never occurs in normal animals; 4) apoptotic cell death in the developing and adult forebrain is mediated by the activation of caspase-3; 5) congenital and acquired hypothyroidism affect the survival and phenotype of the GABAergic striatal neurons; 6) congenital hypothyroidism induces a significant shrinkage of the size of the striatum in the adult; 7) the duration of hypothyroidism (congenital or acquired) appears to differentially affect cell viability, with congenital having more profound effects.